This post, however, is not about the absurdity (or hypocrisy) of criticising the challenge on the basis of clean water shortage in the third world, or the fact that the uncomfortable symptoms of “FB peer-pressure” tend to dissipate naturally over a short period of time, whereas ALS causes an inexorable disabling of all the body’s faculties until the sufferer can no longer breathe on their own, and results in death, always. No, this is about medical pseudoscience at its very, very worst. And I’ve seen it shared by some pretty sensible people, which has been disturbing. To those people:

Please be aware that most articles posted on social media that talk about health, disease or science, are BULLSHIT. A good rule of thumb is to type the author’s name into Google followed by the word ‘skeptic’. Then do the same with the word ‘rational’, ‘quack’ (or ‘quackery’), ‘debunked’ and ‘pseudoscience’. Repeat this process for the name of the website, and key words from in the article.

I was ‘inspired’ to write on the subject of ALS charlatanism by this profoundly misleading article, authored by conspiracy-mongering pseudowhistleblower and all-round crank Anthony Gucciardi. The article is first and foremost a libellous denigration of the ALSA. He couples this with a few references to some cherry-picked studies he either hasn’t read or doesn’t understand, which he uses for the purposes of implying, strongly, that ALS is a disease which can be easily prevented or reversed through diet. Hint: it isn’t. The most flabbergasting aspect of Gucciardi’s article is how outrageously, wantonly, and shamelessly lazy (or calculatedly deceitful?) a mere couple of clicks around the ALSA’s website reveals him to have been.

I’ll be focusing mostly on what Gucciardi has actually written, though I will broaden the discussion at times. I would also point out that numerous members of the ‘alternative’ crowd, such as Joseph Mercola, have posted articles or videos encouraging members of the public not to donate to the ALSA – the whole incestuous ‘alterweb’ is buzzing with them. Take your pick – they are mostly variations on one quack theme: don’t give money to ALS charities; buy our supplements instead.

Disclaimer

What follows is a long article, and no doubt there will be sections that for some readers will represent a case of tl;dr. That’s fine. I just wanted to be as thorough as possible, because that’s what I think this topic deserves. So I’ve said everything I think needed to be said. I could have summed the whole thing up like this: “Gucciardi and his cronies are spreading misinformation about the charity they are publicly slamming, and if you want to verify that for yourself, all you need to do is to do is visit the ALS Association’s website. None of the studies he cites say what he thinks they say and, in any case, knowing a few risk factors for a complex disease doesn’t mean the disease is preventable or reversible. Furthermore, what is he doing citing scientific studies when they come from institutions that are just as (inevitably) tied up with the pharmaceutical industry as the ALS Association is? His article and the principles upon which it is based are a mess of double standards and illogic. He’s out of his depth and I think he knows it. Next!” But if I did that, I’d only end up having to write a patchwork version of my essay in the comments thread anyway. Instead, I will now be able to refer commenters to relevant sections, if they respond in disagreement, having not read them.

Though it includes much more extensive (professional-standard!) cherry-picking, Sayer Ji’s article doesn’t add anything qualitative to Gucciardi’s, so my focus will remain mostly on that. However, this is arbitrary, resulting from the fact that I discovered Gucciardi’s first. I will comment on Sayer Ji’s misinformation campaign at the end, because I think it will be doing more damage than Gucciardi’s, and is arguably a couple of orders of magnitude more disgraceful.

To any scientifically-literate person, especially anybody with an understanding of complex disease (on which more later), it is plain as day that Gucciardi’s and Ji’s take on ALS stems from ignorance and delusion. But I dread to think how many well-meaning people without the necessary background knowledge to see this will have been roped in by their sleazy impersonations of people who know what the hell they’re talking about.

Rebutting attacks against the ALS Association

The opening section of Gucciardi’s article revolves around a pie chart published by the ALSA on their website, displaying the various ways in which their finances were allocated, and in what proportions, over the financial year ending January 2014.

Gucciardi introduces his pseudo-exposé with the heading:

“$95 Million Later: Only 27% Of Donations Actually Help ‘Research The Cure’”

But of course the pie chart tells us nothing about how the ice bucket donations will be used. It tells us how the ALSA apportioned their funds last year, when they had about $25 million to work with. There is no reason to expect the slices of this pie to increase proportionately with respect to one another in the wake of a sudden influx of over $100 million. And besides, there is a button you can press when you make your donation, if you want 100% of it to go to research. The unctuous preface for the paragraph headed by this baseless claim reads, “But don’t just take my word for it”. Well, thanks, Anthony, we won’t.

Since ALS is currently incurable (and care for a patient can cost upwards of $200K per year), one of the single most important resources for patients and their families is access to support, which the ALSA calls patient and community services. In his piece, Gucciardi mentions twice that even more important than supporting local communities “the spread of information.” What, you mean, like, public and professional education, Anthony? You know, that thing represented by the largest slice of the pie you just shat all over?

So, this leaves only two slices that don’t represent one of the ALS Association’s core activities, as declared in their manifesto. These core activities, incredibly, cost money. (I know, right?) There’s a name for the systematic gathering of money. It’s called fundraising. The more you publicise your cause, the more funds you’re likely to raise. Being a businessman, Anthony, presumably you are aware of the costs associated with publicity. One slice left.

Where Gucciardi really goes to town is with administration costs, particularly via his having copied and pasted the salary figures for the ALS Association’s executives, including — gasp! — the CEO’s salary of $339,475. He has this to say on the matter:

“And let’s be clear: I am a huge proponent of prosperity and business expansion. When it comes to private business and commerce, it benefits us all to see growing numbers among a company and its members. This, however, is not the case for a ‘non-profit’ organization that is based around the concept of ‘searching for the cure’ and ‘funding research’ as its primary goal. Especially when this organization is being funded with close to 100 million dollars through a viral social media campaign in which it appears no one truly took the time to investigate the very company they are shoveling their assets into.” [Emphasis his]

Congratulations, Anthony, on finding such a convenient way to cover your back: It’s perfectly virtuous to want to earn a large salary, but if you accept one and play an instrumental role in the running of an organisation that works directly to improve the lives of other people, then you become immoral. Duh!

Good logic right there.

I fail to see how it could be the case that “when it comes to private business and commerce, it benefits us all to see growing numbers among a company and its members“, but when it comes to the non-profit sector, it doesn’t. I’d say that the downstream effects of charity CEOs having substantial financial incentives are probably much more beneficial “to us all” than are the consequences of private business CEOs having them. Gucciardi seems to be expressing a feeling, apparently shared by many, that someone who heads a charitable organisation ought to have no desire to earn a good living – that there is something hypocritical about accepting a good wage if you’re receiving that wage from the non-profit sector. Personally, I’d say that someone who earns a six-figure salary heading a furniture (or supplement) company deserves fewer ethical brownie-points than someone earning the same amount of money via activities that directly help people with a crippling disease. As devil’s advocate, I’d turn the tables and say of those working in the profit sector that not only are they not working to improve the lives of others, but they’re also accepting a large wage! Shocking!

If you object to large salaries per se, given how many people in the world live in poverty, then I’d suggest that your campaigning efforts would be better directed towards people who have hundreds of billions of dollars squirreled away in vaults, doing nothing; you know, that 1% of people who control half of the world’s ‘wealth’, in the form of little bits of paper. If you’re coming at this from a Marxist perspective (which Gucciardi clearly isn’t, since he expressly doesn’t object to “growing numbers” in the profit sector) then forgive me but you seem to be forsaking one of your own core principles: what $300K a year can buy you under our current system is within what the world could theoretically provide for every person living in it. If you’re attacking this individual CEO, you’re doing it because the opportunity to do so has been served up for you on a plate; not because you’re an activist. Every minute you spend attacking this person is a minute you could have spent campaigning against real corporate juggernauts. It’s a simple case of lazy scapegoating.

Besides, the moral status of this one person is not the relevant issue. We have to think of this from the perspective of the ALSA, which has an official moral duty to perform as well as it can. To make a large-scale charity as innovative and successful as possible, you need a leader with maximum experience, business know-how, connections, and an intimate knowledge of the sector’s infrastructure and dynamics, working full-time. In other words, you need a CEO who can command a high salary. One could just as well argue that it would be immoral for the ALSA to scrimp on such an integral component of their organisation. The ALSA do not set salary standards – it’s not their fault that high-level CEOs are in a high wage-bracket.

The salaries of our executive staff are in line with the job markets where they are located—and in line with those of other national charities. Salary review is part of the accreditation process for the watch dogs mentioned above and is a requirement of the National Health Council (NHC), of which we are a member. In fact, The ALS Association is the only ALS charity that has qualified for membership. Read what this journalist has to say about The ALS Association’s executive salaries: “they are all well within the range of nonprofit salaries; the compensation for ALSA’s CEO compares favorably with that of his peers, including some who run low-performing nonprofits.” [Emphasis my own.]

As his final word on the way in which the ALS Association spends its funds, Gucciardi references Sayer Ji, who he says

“points out in his breakdown of the ice bucket phenomenon [that] even the smaller portions spent on ‘research’ for ALS are actually going towards pharmaceutical interventions and the pharmaceutical industry at large.” [Emphasis my own]

So, after all that fuss about not enough money going towards research, Gucciardi reveals that he doesn’t support research anyway. Sigh.

In any case, this statement is absolute bullshit. There is no evidence that the ALSA give money to “the pharmaceutical industry at large”, much less that the money they spend goes there rather than on research.

Nearly all of them have been awarded to researchers looking at care protocol and equipment. Things like how to measure respiratory impairment and assist ventilation in the best way, how best to support patients nutritionally, keep their muscles moving, support their families, and generally maximise their quality of life. In other words, NOT pharmacological interventions. Of the eighteen grants awarded over the last several years, as far as I could tell, only two have been for pharmacological studies. One of these looked at whether the substance used in botox treatments could help prevent patients drooling, and the other (prepare yourself for some truly savage irony) was on…

Amazing, isn’t it? The alternative crowd devote all that time to criticising “the medical industry” for not funding research on cannabinoids, because “pharma companies aren’t interested in something they can’t profit from it”. And then they’re so blinkered in their approach, so damned lazy, and so lacking in even the measliest morsel of integrity that they end up actively dissuading people from supporting one of the very few institutions that actually happens to have done so. One of Gucciardi’s other ‘articles’ is entitled Cannabis Treatment Threatens Deadly Painkiller Industry. The THC study that the ALSA funded through their grant scheme was on whether it could reduce painful cramps in ALS sufferers. This calls for a *facepalm*. Ouch, that one’s going to bruise.

The ALSA are also currently recruiting for a clinical trial they’ve funded to ascertain whether THC helps with spasticity. I found it using this search tool (via the ALSA’s website), which can pull up a list of all the clinical trials they’ve ever funded. Again, only a small fraction of these studies are on pharmacological interventions, because, unfortunately, our understanding of ALS is still not good enough for there to be lots of potential drugs discovered and ready to test. Part of the reason for this is that ALS is a rare disease, so it’s not an attractive research area for pharmaceutical companies. Which is precisely why charities like the ALSA end up contributing towards the cost of clinical trials on the very few drugs that are worth investigating.

The two main prongs of argument against pharmaceutical companies surround 1) transparency and 2) profiteering. Regarding transparency, pharma studies that have been part-funded by an independent organisation like ALSA should garner less, not more, suspicion than those which are purely industry-funded. And with respect to profiteering, if you don’t like the fact that medicine is tied up with this, then you need to be campaigning against our political system in the large – against the privatisation of medicine, and against capitalism, at least in its current form. Campaigning against pharmaceuticals per se, like the alt-med crowd do, is bad reasoning at best, and outright hypocrisy at worst, namely when it concludes — as it usually does — with “so, buy our health products instead!”

Many of the arguments used by pro-alt-med bloggers and commenters break down when you consider countries that offer universal healthcare. But wherever you’re from, and whatever you feel about the privatisation of medicine, or capitalism in general, pharmaceutical companies are currently the only organisations that are able to properly test and manufacture drugs, and drugs are what ALS sufferers desperately need because unfortunately…

ALS Cannot be Cured ‘Naturally’

We should start this section with a brief consideration of complex diseases, which can be contrasted with ‘simple’ Mendelian disorders with clear inheritance patterns like Huntington’s disease, that result from a single mutation with powerful a effect whereby if you have the gene, you will get the disease.

Heart disease is an archetypal example of a complex disease. It is weakly associated with heaps of common genes, as well as various environmental risk factors that seem, statistically-speaking, to slightly increase a person’s risk of becoming a sufferer. Like other complex diseases (such as arthritis, most cancers, and ALS), it doesn’t usually have clear, straight-forward inheritance patterns, though it does often run in families.

However, as with cancer, where some rare genes confer a greatly increased — or even 100% — risk of developing disease, there are some rare genes which are very strongly associated with ALS and, like all genes, they are heritable. Inherited forms of ALS are called ‘familial ALS’, and account for about 10% of all ALS cases. Roughly half of these cases can be explained by around 17 known genes. (Some are discussed by the ALSA on their website, and a comprehensive database of all genes which have been found to be linked to ALS can be found here.)

To give an example, depending on which population you look at, between 20% and 40% of familial ALS cases are caused by inherited mutations (in this case, repetitions) of a gene called C9ORF72. (An inherited mutation is often just called ‘a gene’, which can be confusing.) This gene was discovered recently through studies conducted by two different research groups, independently of each other. Both were funded by the ALS Association.

Importantly, however, as this twin study, and this (free) paper on ALS as a genetic disease point out, the distinction between spontaneous and familial ALS is largely artificial. This starts to make sense if you think of ALS-causing genes as sitting on a continuum of effect-size, or ‘penetrance‘. At one end are genes with complete penetrance, which are certain to manifest in ALS, like the C9ORF72 repeat expansion discussed above. As you move along the spectrum, certainty becomes likeliness, which gradually peters out, with associations becoming ever weaker. (Also, de novo mutations — occurring spontaneously during the very early stages of development, rather than being inherited from a parent — can produce the same effects as inherited ones.)

The evidence we have points towards a ‘liability threshold’ model of ALS, under which disease manifests only once a critical tipping point has been reached. Everyone is born with a pre-determined genetic liability and, over time, this liability can be modulated by the environment. The fewer environmental risk factors you are exposed to, the less likely you are to reach the tipping point, provided your initial genetic liability, or ‘genetic load’ isn’t so high in the first place as to completely flood the effects of environmental influences.

There is an enormous variety of ways in which one might reach the threshold. The ‘easiest’ way is to carry a gene from right at the top end of the effect-size spectrum. But you could also do it by carrying lots of genes from somewhere in the second quartile of the continuum, and then exposing yourself to some environmental risk factors. Or you could do it by carrying a very, very large number of genes right from the low end of the spectrum.

And here’s the thing. It is much, much, much easier to identify genes that greatly increase disease liability, compared to genes that only increase it a little bit. These big bruisers ‘stand out’ when you compare large enough samples of cases (ALS patients) with samples of controls (people without the disease). But the potentially huge number of mutations that ever-so-slightly increase ALS risk sink into the background and are virtually impossible to distinguish from random ‘noise’, since they are each found almost just as often in healthy controls as they are in ALS cases – it is their collective presence in a person’s genome that causes disease. However, these low-penetrance genes are just as heritable as genes with high or complete penetrance.

Genetic material is shuffled and split in half during reproduction. In the case of one, fully penetrant gene that is sufficient to cause ALS without the ‘help’ of others, or of environmental factors, since a sperm or egg either ends up with this gene or not, the resulting person is either destined to develop the disease, or not, manifesting in a classic Mendelian inheritance pattern (autosomal dominant, for C9ORF72 mutations). When we’re talking about a large number of low-penetrance genes, however, a sperm or egg could, by chance, end up with anything from 0% to 100% of those genes (50% on average). This can explain the fact that we often see striking familial clustering of ALS cases, despite the fact that none of the 17 big genetic players are contained within their DNA – something that is enhanced by the fact that people from the same families tend to have more shared environmental influences than two people picked at random.

You could also inherit ‘sporadic’ ALS in the absence ofany family history, if the combination of genes you inherit from your parents happens to place you at or beyond that threshold, even though neither of them were particularly close to it themselves.

To make things even more unpredictable and hard to shed light on, genes modulate other genes. And they often act differently depending on which other genes they end up with. Different versions of the same gene can also interact differently with the same environment and, conversely, a single gene variant can act differently in different environments. It is feasible that the same environmental factor could increase or decrease your risk of ALS, depending on what your genome looked like.

All this ferocious complexity is part of the reason why studies looking at environmental risk factors for ALS have been inconsistent in their results, with some finding associations, and others failing to reproduce these. It is also immensely difficult to tease out causation in a world teeming with correlation, or to eliminate the numerous forms of bias which can so easily creep into observational studies (as opposed to randomised, controlled trials). Finally, publication bias skews the picture too. Some associations that have been flagged up will turn out to be spurious; others will turn out to be explained by other, unseen variables. Others won’t be found, even though they really do exist. Please keep this in mind as you read the rest of this article.

Gucciardi’s cherry-picking trip

Starts with:

“Numerous studies available through the United States National Library of Medicine have demonstrated the natural preventative effects of key substances…

Vitamin E: Shown by research to exhibit a whopping 50-60% decreased risk of developing ALS when taken alongside powerful polyunsaturated fatty acids.”

Irrespective of the quality of the vitamin E/ALS research he cites, a reduced risk does not equate to a preventative, and in any case applies at a population level, though as we’ve seen, some individuals are born with a 100% risk of developing ALS, regardless of environment. What about them? Don’t they deserve access to the drugs that might be discovered through pharmacological research?

Critically evaluating individual studies was not what I set out to do here. I mentioned earlier that there are various inherent weaknesses of observational studies, and I would have left it at that, but since this study is being flaunted so widely (it features on GreenMedInfo too, and therefore on scores of other popular alternative/conspiracy websites), I couldn’t help but feel that a brief critique was warranted.

Not that the authors claim it is, but we should be clear that this study is not a randomised trial. The researchers didn’t give one group of people vitamin E and polyunsaturates and one group a placebo and then wait to see whether either group had higher rates of ALS. They sent questionnaires to patients in clinics, both ALS and healthy, asking them to “recall their dietary habits during the period 1 year before the onset of muscle weakness or bulbar signs”. Then, amongst 15 micronutrients, they looked for associations with ALS. The authors apparently did not apply a correction for multiple comparisons, which is a serious oversight, and it makes the study seem like something of a fishing expedition, since the more things you compare, the more likely you are to get a ‘significant’ result, just by chance. This is called a ‘false discovery’. One would expect the false discovery rate (FDR) to be pretty high with this many comparisons.

There is a later vitamin E study, cited by Sayer Ji but not by Gucciardi, that pools five datasets (including the one just discussed). However, it too appears to lack statistical rigour. The researchers found that, overall, vitamin E did not reduce risk of ALS (in fact, there appeared to be a slightly higher risk of ALS in vitamin E supplement users – though to be clear, this does not provide evidence that vitamin A actually increases risk of ALS). However, when they then looked at the (very small!) datasets that included information on the duration of use, they found a significant trend. But to get their significant results, it seems that the authors had to run various different analyses on their data, reorganising it for the purpose (and apparently without making FDR adjustments). For a discussion of the problems with re-arranging and re-analysing data, see chapter 4 of Ben Goldacre’s Bad Pharma, especially the sections called Dodgy subgroup analyses and Dodgy subgroups of trials rather than patients.

From that chapter: “If your drug didn’t win overall in your trial, you can chop up the data in lots of different ways, to try and see if it won in a subgroup: maybe it works brilliantly in Chinese men between fifty-six and seventy-one. This is as stupid as playing ‘Best of three … Best of five … ‘ And yet it is commonplace.”

The most recent study on vitamin E and ALS was a randomised clinical trial conducted in Finland, and the researchers did more than just measure ALS risk – they also measured subjects’ serum vitamin E levels (how much of it people had in their blood) at the beginning of the trial. Overall, they found that vitamin E supplementation did not significantly mitigate risk for ALS. However, when the data was split in half along the mid-point (median) to produce one group of subjects who, prior to the trial, had higher vitamin E serum levels and one group who started with lower levels, they found that in the lower group, supplementation did confer a reduction in risk. But the study doesn’t tell us about the finer-grained relative-risk distribution; the data was simply cut in half along the mid-point.

The interpretation of this study most likely to be correct is that ALS is associated with vitamin E deficiency and that only the people right at the bottom of the low-serum group (people who had levels far lower than the median) benefited from vitamin E supplementation. This seems most likely for two reasons:

This study looked at ~ 30,000 people. The fact that their overall results weren’t significant, despite such a large sample size, suggests that there were very few people within it for whom supplementation had any effect (which is parsimonious with the fact that vitamin deficiency in 1st world countries is rare), but that in those people, since there was very a real initial risk to begin with, vitamin E had a significant enough effect to be detectable even when diluted by the rest of the group.

In other words, the most rigorous study we have on vitamin E and ALS does not provide any evidence that the average person will reduce their risk of ALS by increasing their vitamin E intake, despite Sayer Ji having included it in the collection of cherry-picked articles he has put together and posted on his supplement-pushing website.

Gucciardi continues:

“Vitamin B12: Demonstrated by scientific study to be highly beneficial in the aid and understanding of ALS. In fact, PubMed research specifically reveals the integral usage of vitamin B12 in ALS research:”

Now, perhaps this is petty of me but I can’t resist pointing out how silly referring to a study as “PubMed research” makes Gucciardi look. PubMed is a search engine. Not a research outfit. And if that’s what he thought it was, again, what was he doing citing its research? “PubMed research” is a wellspring of industry-funded studies.

This study did not demonstrate vitamin B12 to be “highly beneficial in the aid and understanding of ALS”. What does that even mean? The idea that the study “reveals the integral usage of vitamin B12 in ALS research” came from Gucciardi’s head (or arse, depending on how you look at it). This wasn’t a study about studying ALS and how useful vitamin B12 has been for that. It was a study with a very specific remit, looking at the effect of ultrahigh-dose vitamin B12 on compound muscle action potentials (CMAP) in ALS sufferers. To achieve significant results, the investigators had to give patients roughly 17,000 times the recommended daily allowance (RDA). There is little evidence that vit B12 is toxic even at this level, but it’s all by the by really, since the authors of the study are careful to point out that “CMAP improvement, as demonstrated in this study, needs to be interpreted with caution, because it may not reflect clinical muscle wasting or weakness. Moreover, this transient effect does not necessarily lead to retardation of the disease process.”

In other words, this study does NOT provide evidence that vitamin B12 helps to reduce the risk of getting ALS, nor does it provide evidence that vitamin B12 prolongs the lives of those who have ALS. And it certainly, absolutely, totally does not suggest that vitamin B12 can cure, or will ever be able to cure, this disease.

“And the list goes on”, says Gucciardi.

(What, you mean, the list of studies that don’t say what you think they say?)

He goes on: “Looking to the research we find an extensive list of culprits that can be identified and reduced, including:

1) Pesticides: Not mentioned by the ALS Association, a number of studies have drawn links between ALS and pesticide exposure.”

It’s really, really hard not to explode with swear-words at this point, as Gucciardi flaunts, yet again, his scandalously irresponsible failure perform a few clicks around the website of the organisation he is publicly denigrating. This really is an unambiguous case of

“2)Lead: Often contaminating the food supply and foreign products, 4 studies have demonstrated a relationship between lead and ALS at large.”

In 2009, a systematic review of the evidence surrounding lead as a risk factor for ALS was published. It looked at 50 studies on lead, mercury, aluminium, cadmium, manganese and selenium, and found no evidence of a causal relationship between any of these and ALS.

Since then, some other studies have supported a link between lead and ALS, but the researchers make it clear that this excess risk could by no means be enough to account for ALS, representing just one factor amidst a sea of genetic and possible environmental influences. Indeed, if lead were a particularly powerful causative agent in ALS, we would expect this to have shown up unambiguously the 2009 review. Furthermore, lead exposure in developed countries (like the ones in which readers of Natural Society and Storyleakreside) has been greatly reduced through public policy, especially during the last few decades, as a result of lead-reduction programmes.

“3)Statin Drugs: You may already be well aware of the dangers surrounding statin drugs, in which case this may not surprise you. ALS has been identified as a possible side effect of these drugs that aim to reduce cholesterol.”

This review of all the studies looking at statins and ALS points out fundamental problems with the available studies finding an association, including several very serious limitations of the study Gucciardi links to, which the authors themselvesacknowledge, conceding that their research does not provide actual quantitative support for an association between statins and ALS. The paper most certainly does not make the claim that ALS is a “side-effect” of statins. Grrrrrrr!!!

The authors of the 2009 review point out that the only rigorous study on statins and ALS to date did not find an association, which is parsimonious with the observation that, since the 90s, statin use amongst 60-to 69-year-olds has gone up from 5% to 50% in men and 33% in females, and yet, when increased life-span is taken into account, there is no evidence that rates of ALS have risen since then.

Anthony wants us all to know, in no uncertain terms, just how thoroughly bloody wonderful he is.

He writes:

“Earlier this year, I found out about a Washington native named Ben Charles whose charity had been shut down by beauracratic [sic] government officials — even going as far as to threaten Ben with arrest for feeding the homeless on the streets of Olympia. Concerned about this issue, I further reached out to Ben back in early December of 2013, documenting the government crackdown on his initiatives and others.

Later that month, I gave another church that was targeted by the government for handing out turkeys on Thanksgiving a $1,000 donation in order to purchase additional food items (specifically turkey) and distribute it among those who needed it in the area — a proverbial middle finger to the bureaucratic park rangers and officers who sought to shut them down. This was also done as an initiative to drive others to do the same.

Now, amid yet another social media donation campaign that has led to almost 100 million going ‘towards the cure’, I am inspired (and want to inspire others) to give to a charity that really gives directly to the people it seeks to serve. That’s why I am giving $2,000 to Ben Charles and his grassroots ‘Crazy Faith’ food program in Olympia, Washington in order to help feed hundreds of homeless individuals on the streets with healthful food items.”

[Emphasis his!!!]

When I read this ingratiating report of how much money Gucciardi has personally given to charity (a report that Storyleak (ie. Gucciardi himself) has made into a headline that appeared as an enormous banner on the site for a couple of weeks), I wondered whether the whole article had been a pretext to lord his magnanimity over us.

I learnt in Gucciardi’s biography (see note at end of article) that one of his favourite bible verses is Psalm 94:16: “Who will rise up for me against the evildoers? or who will stand up for me against the workers of iniquity?” [sic]

I wonder what he feels about Matthew 6:1-4: “When you give to the needy, sound no trumpet before you, as the hypocrites do in the synagogues and in the streets, that they may be praised by others. Truly, I say to you, they have received their reward. But when you give to the needy, do not let your left hand know what your right hand is doing, so that your giving may be in secret.”

Gucciardi concludes:

“Whether or not you have the funds available to support your local communities, what’s even more important is the spread of information. If everyone donating to the ALS Association actually took the time to share key articles such as those highlighting the dangers of ALS-linked toxic substances, or those discussing the power of natural alternatives to ALS treatment, millions would be helped within hours.” [Emphasis his]

I hope that this article has made it clear that what Gucciardi is doing, and encouraging others to do, is hurting people, rather than helping them, because what he is spreading isn’t information but misinformation.

Sayer Ji, whose fast-growing website has an estimated net worth of $189,000, is getting around 90K page views per day, and making around 8K per month in advertising, is running a particularly appalling ALS misinformation campaign, apparently hand-in-hand with Joseph Mercola. In this article, the headline screams “60+ Natural ALS Cures the “Ice Washing” Campaign Isn’t Funding!” (Here’s another one — the one Gucciardi links to — where he makes most of the same nonsense claims.) To support his claim that ALS can be cured in 60 ways, he refers you to a “GreenMedInfo’s free ALS research PDF”, where he has listed all the scientific papers he’s cherry-picked that sport titles seeming, superficially, to support his view that ALS is something that can be prevented/reversed ‘naturally’. It’s hard to find the words to describe just how criminally unethical this is. The research written up in these papers has been conducted by scientists who understand that ALS is a complex disease. Not one of these papers contains the claim that ALS is curable, and there is no doubt that they would be horrified to see their work being exploited in this way. Compiling them, in a catalogue, under the banner of “ALS cures”, knowing full-well that none of his subscribers will read or be able to understand them, and almost certainly having not read them himself, is a heinous abuse of science, and of the trust of his readers. It’s enough to make you weep. Because of this document, and because of their so-called “cumulative knowledge database“, a scarily sophisticated-seeming system for disguising their woefully unscientific enterprise with apparent scientific credibility, I vote GreenMedInfo for most inhumane, despicable website on the net.

I wrote this article for various reasons, summed up here. But in particular, I wrote it because…

Neurodegeneration quackery harms patients

I spoke to neurologist Jonathan Howard about the damage that this kind of charlatanism does to actual patients suffering from ALS, whom I think for Gucciardi and Ji are more like an imaginary concept than real people. Here is what he said:

Many of my patients with chronic and untreatable neurological diseases (ALS, MS, and Parkinson’s disease to name a few) embrace unproven treatments. I get it. These are desperate people dealing with terrible diseases. These “treatments” are usually harmless.

However, there is a subset of patients who embrace only quackery for diseases such as MS, where there are effective treatments. (And of course, those same quacks are happy to take their money.) The same will undoubtedly be true of ALS, once effective treatments are available. Some patients spend tens of thousands of dollars on unproven treatments, enriching unethical, modern-day snake oil salesmen. These are the most obvious harms done by charlatans like Gucciardi and Ji.

But what is less appreciated is the terrible psychological price paid by patients who feel they ’caused’ their disease, or are to be blamed for its worsening. Some of my patients feel responsible for every downturn and berate themselves endlessly for it. Powerlessness in the face of an unrelenting disease is inherently difficult to come to terms with. However, being told and able to accept that they did not cause their disease — and have little control over its course — can be profoundly liberating. It can allow people to enjoy themselves as much as possible without shame or guilt.

Additionally, telling patients that ‘natural’ cures exist but are are being suppressed by Big Pharma serves to make some patients paranoid and bitter. I suspect Gucciardi and Ji know this, and it is easy for them to exploit when they are not faced with the challenge of seeing these patients face-to-face on a daily basis. In adding fear and guilt to their already profound physical suffering and poisoning the relationship between doctors and patients, they open the door to their highly remunerative quackery.

*If you do read Gucciardi’s biography, I would like to draw your attention to sceptical literature on ‘chronic lyme disease‘. I’d also point out that normal treatment for lyme disease does not include steroids. Steroids only become appropriate if the lyme disease has caused an auto-immune response like arthritis. In general, steroids would be a bad thing to give to someone suffering from a bacterial infection, since they suppress the immune system. Make of that what you will.

With special thanks to Joseph Bundy and Jonathan Howard, for being excellent sounding boards and offering helpful suggestions. It was extremely useful to be able to discuss vitamin E research with Joseph, and to have Jonathan’s first-hand account of how quackery harms patients with neurodegenerative diseases.

We’ve had numerous requests for a post on the idea that dental cavities can be cured through diet. It’s a popular theme at Natural News, and Wellness Mama, along with many other websites offering “wake-up calls” and extolling the virtues of living “naturally”. From what I can gather, the enthusiasm with which the notion of “healing” cavities at home is currently being promulgated seems to be owed in large part to a book with the amusingly imperative title, Cure Tooth Decay, published in 2010 by Ramiel Nagel. It is loosely based on the work of Weston A. Price (on whom more later). All of the holistically-flavoured articles I’ve come to read on this subject mention Price, and most of them also draw from studies conducted by dentists Edward and May Mellanby. IFHP has received two or three messages from readers directing us to Natural News’ take on the subject (repeated verbatim at many other online locations). The sources it cites are: itself (twice), Wellness Mama and the Weston A. Price Foundation. Incidentally, regarding ‘wellness’, John E. Dodes, D.D.S., a dentist and outspoken critic of ‘holistic dentistry’, has noted that this is “something for which quacks can get paid when there is nothing wrong with the patient.” This note deals mostly with the claims made by NN, but also touches on some of those found elsewhere, on websites of the same bent.

So, first things first: I am not a dentist. While I have done everything I can to make this as accurate and comprehensive as possible within a reasonable amount of time, I would like to make it very clear from the outset that suggestions for improvement, particularly by dentists, are very much welcomed. First, here’s a brief word on the theory of tooth decay accepted by mainstream dentistry.

Tooth enamel is a dense tissue made mostly of hydroxyapatite, a molecule comprising calcium, phosphorus, carbon, hydrogen and oxygen. Being a-cellular, it is in fact a dead tissue, as is dentin – found directly beneath the enamel – which is also a-cellular.Enamel is is 96% minerals. (Dentin is 70%.) In the mouth, enamel is subject to constant cycles of softening and hardening. After eating foods containing fermentable carbohydrates such as sucrose, glucose and fructose, residues left in the mouth are broken down by oral bacteria, which produce lactic acid as a waste product. This local reduction in pH increases the solubility of hydroxyapatite, which begins to dissolve, in a process calleddemineralisation. However, once the sugar has gone and the pH has risen again, mineral ions suspended in the saliva are reuptaken by the tooth enamel. This part of the cycle is called remineralisation. Nowadays, the remineralisation process is enhanced by water fluoridation. Here is a useful article discussing fluoride’s multifaceted role in remineralisation: http://www.accessscience.com/studycenter.aspx?main=13&questionID=4858

The more frequently teeth are exposed to fermentable carbohydrates (particularly sucrose, see later) and acidic food, the less time the teeth have for remineralisation before they are subjected to the next round of demineralisation. As such, tooth decay (also known as ‘dental caries’) occurs when the rate of the latter exceeds that of the former, and lesions of softened, pitted enamel start to form. These weak areas represent the first stages of decay, and are sometimes known as ‘microcavities’. The good news (and herein lies our kernal of truth) is that, if treated properly with remineralising pastes, the development of these lesions can be reversed. However, once tooth decay has penetrated all the way through the enamel, forming a ‘true cavity’, this is irreversible. Why? because since enamel is a-cellular, it cannot grow. It is formed early in development by the ‘enamel organ’, which recedes by the time teeth erupt. Filling a true cavity is particularly urgent because, since the dentin is less mineralised (and therefore less resistant to the acid produced by oral bacteria), the decay process typically mushrooms out rapidly once it reaches the dentin, in a way that is sometimes described by dentists as a “cavity bomb going off inside the tooth”.

It should be borne in mind, then, that there is an important, qualitative difference between microcavities and the kind of cavities shown in this very popular picture (http://www.healthy-holistic-living.com/images/healcavities.gif), which accompanies many of the online articles in question. Later in this note, we’ll investigate the (misrepresented) source that has been exploited to gloss over this difference and promote the slap-dash notion that “cavities” can be “healed” at home.

Now for some direct quotations from Natural News:

The world is slowly waking up to the fact that, when you give the body what it needs, it can heal things we previously thought were impossible. A fine example of what is often deemed as an incurable health problem is dental cavities, but extensive research is now becoming more public about the true nature of tooth decay and the fact that there are proven remedies that can remedy it.

Starting with a sweeping statement that implies all illnesses result from not giving the body “what it needs”, is an obvious red flag. Even if it were theoretically true that all disease could be prevented by feeding the body in such a way as to match supply perfectly with demand, with the ingestion of nutrients in exactly the right measurements, at exactly the right times, not enough is known about minute-to-minute body chemistry to put such a regime into action. And that’s before considering that every human body is different. This attitude, moreover, is implicitly dismissive of congenital diseases such as cystic fibrosis, a very serious condition caused by the unlucky pairing of two dodgy mutations from mother and father, and which requires an arduous daily schedule of treatment with drugs and mechanical intervention to prevent childhood death. This opening statement is redolent of willful ignorance and unconditional distrust in medicine, and we should probably expect what follows it to be flavoured with an antiscience bias, even if it originated somewhere other than Natural News.

The lies perpetrated about tooth decay:

According to the American Dental Association, the reason we have tooth decay is as follows:

“[Tooth decay] occurs when foods containing carbohydrates (sugars and starches) such as milk, pop, raisins, cakes or candy are frequently left on the teeth. Bacteria that live in the mouth thrive on these foods, producing acids as a result. Over a period of time, these acids destroy tooth enamel, resulting in tooth decay.”

There are a few problems with this theory, including:

Groups of indigenous people who had fermentable carbohydrates stuck on their teeth all the timethat did not brush or floss were mostly or completely free of tooth decay.

This is a reference to the work of Weston A. Price, a dentist who has inspired a lot of praise, particularly in ‘holistic’ circles (see http://www.westonaprice.org/) and a fair bit of criticism, too. See, for example:

The Quackwatch article is arguably a little harsh, and it is important to note that Price’s work has often been pilfered and warped by others to promote dodgy theories that actually bear little resemblance to his own research. The Wiki articles on him (and the dubious foundation inaugurated in his name) are worth a read.

In Nutrition and Physical Degeneration (1939), Price gives an account of his observations of “primitive” peoples from various indigenous populations around the world, reporting that they were remarkably free of diseases afflicting Westerners, including dental caries. One of his conclusions was that Western food preparation methods were stripping away nutrients, resulting in deficiencies which, he proposed, explained tooth decay (and other diseases). During his research, Price observed that these indigenous groups, when they moved towards more Western diets, began to develop dental caries, interpreting this as support for his theory.

Price did in fact believe that sugar was a significant cause of dental caries, but hypothesised (incorrectly) that its cariogenic (tooth decay-inducing) action was to reduce the amount of minerals absorbed by the body. It wasn’t until the 1940s and 50s that the actual role of sugar in tooth decay was discovered, so this was a valid hypothesis at the time. Full appraisal of Price’s work is far beyond the remit of this note but, in short, it seems he did some interesting research which perhaps fell short on scientific and quantitative rigour. Some quick points:

Malnourished people, overrepresented in Price’s subjects, get fewer dental cavities, as they experience longer periods of time without dental exposure to food.

The serious increases in tooth decay experienced by indigenous people who then gained access to Western foods could be explained by overindulgence, by virtue of sugary foods being a novelty to them.

Price’s research was conducted before the time of vitamin-fortification of Western processed carbohydrates, before the time of water fluoridation, and during a time when tooth decay in the Western world was almost at its highest in history (it reached a peak during the 50s and 60s). For a full-text review of the history of dental caries, published by Nature,see http://www.nature.com/bdj/journal/v191/n9/full/4801214a.html

Despite the controversy surrounding Price’s work, it is actually compatible with a sugar-centric theory of tooth decay.

I have not been able to give the time it would take to read Price’s entire book, but after the research I’ve done around this subject, it seems unlikely that he claimed his subjects “had fermentable carbohydrates stuck to their teeth all the time”, as reported by Natural News.

Bacteria do not consume processed sugar or flour because of the lack of nutrients in them

This is a bizarre statement, made, Naturally, without any supporting reference. There is ample evidence that sucrose, the molecule constituting refined sugar, is eaten by bacteria in the mouth. De-germed (processed) flour contains less (though not nothing) in the way of vitamins, minerals and protein, but is full of polysaccarides, which can be digested by oral bacteria. In any case, the mouth contains a multitude of essential nutrients with which bacteria can supplement their diets. Here are a few references to support the role played by sucrose in caries-formation:

Another, related angle of attack (not included in the NN article) comes from Cure Tooth Decay by Ramiel Nagen. It is repeated in various online articles similar to the one from Natural News. It goes like this:

[Mainstream theory of tooth decay] further dissolves because white sugar actually has the ability to incapacitate microorganisms since it attracts water. In a 20% sugar solution, bacteria will perish. Yes, bacteria are present as a result of the process of tooth decay, but a lot of sugar at once will destroy them. If dentistry is correct about bacteria, then a high sugar diet should eliminate them.

Nagen clearly reckons he’s delivered a real blow with this one. To somebody who has never studied biology, perhaps it sounds like the kind of simple, razor-sharp idea that seems so obvious when voiced that everyone says, “why didn’t I think of that?” Only, this idea is toosimple. It’s one thing to plonk a blob of bacterial cells into a beaker of sugar solution and leave them there, out on a limb, floating around in an abyss with nowhere to hide. As long as the percentage of solutes in the liquid contained inside the cells is lower than the percentage of solutes contained outside them in the external solution, osmosis will ensure that the cells’ watery insides are sucked out, desiccating the little blighters as molecules strive towards equilibrium from both sides of their outer membranes. (http://en.wikipedia.org/wiki/Osmosis) But this lab situation is completely different from the one going on in the human mouth, which doesn’t have smooth glassy surfaces, for one thing. The bacteria in the mouth are established residents. They’ve worked their way into all the nookiest nooks and the cranniest crannies, living in gooey bundles, all huddled up together, nice and cosy. They nuzzle between teeth and ensconce themselves under the harbourage of the gum-line. They squelch around in a caggy spread on the rough, grainy surface of the back of the tongue. Most importantly of all, to help them nuzzle and congregate thus, oral bacteria manufacture an extrapolysaccharide (EPS) slime, also known as a biofilm, using broken-down sugar. This EPS acts as a protective sheath against dessication, holds them together, and keeps them glued to their terrain. Biofilms are why dentists stress the importance of mechanical cleaning with brushes and floss – your antibacterial mouthwash might have “kills 99% of oral bacteria” printed on it, but this kill-rate is likely based on tests with bacteria unprotected by biofilms. When a host human chomps up a cake, the sugary, masticated stodge might feasibly break through some patches of bacterial biofilm, in a similar way to a toothbrush, displacing some of the unlucky bacteria on the outskirts of the huddles, and dragging them, stomach-wards, down the oesophagus. But once the cake-eating eating has stopped, the plentiful remaining bacteria will of course begin spreading over the fermentable residue, digesting it and multiplying afresh.

Foods that bacteria like to eat, such as milk, vegetables, meat, fish and fruit, are not commonly implicated in causes of tooth decay.

Lactose does not appear to be as cariogenic (decay-inducing) as other mono- and di-saccarides. It also tends to be consumed in the presence of other food components such as proteins, fats, and minerals from milk and other dairy products, which act as a buffer, minimising its carious impact. Milk and other dairy products also contains calcium phosphate and casein, both of which aid in the remineralisation process. Fruit, which contains fructose, glucose and some sucrose, doesn’t seem to be a major player in tooth decay, though its acid content can be a cause of tooth erosion, particularly in juice-form, which can increase susceptibility. Something not acknowledged in the NN statement above is that people who eat lots of fruit also probably tend to eat fewer doughuts, meaning that their overall sucrose-intake may be lower. It’s worth pointing out, also, that there is a staggering diversity of bacterial species, some of which have even evolved to digest radioactive material. The phrase “bacteria like to eat” fails to acknowledge the fact that different species of bacteria have different tastes. A class of bacteria called the mutans streptococci represent the main culprits in tooth decay. Of these species, S. sobrinus and S. mutans are the most highly associated with carious lesions on the teeth. The reason sucrose (not found in high concentrations in milk, vegetables, meat, fish, or even fruit) is the biggest dietary factor in tooth decay is because these bacteria specifically rely on it to manufacture sticky, long-chain molecules called glucans, the main ingredient of EPS, discussed above. Thus, the idea that some “foods that bacteria like to eat” are not implicated in tooth decay is not at odds with the modern theory of tooth decay – none of the foods listed in this bacterial tasting menu, à la Natural News, are particularly high in sucrose. See the following papers for further reading on the cariogenicity of lactose and fruit.

So if the modern explanation of tooth decay is not accurate, what is actually the cause of tooth decay?

What actually causes tooth decay

Tooth decay, as researched by Dr. Weston Price and other dental pioneers, boiled down to three factors:

Not enough minerals in the diet.

Not enough fat-soluble vitamins (A, D, E, and K) in the diet.

Nutrients not being readily bioavailable, and your intestinal system not properly absorbing them.The presence of phytic acid largely influences this factor.

Over a period of time, if your diet lacks vitamins and minerals from a poor diet and/or contains high levels of phytates (from grains, seeds, nuts, and legumes), the blood chemistry and the ratio of calcium and phosphorous become out of balance, which results in minerals being pulled from bones, causing tooth and bone loss.

So, the long-standing belief that sugar causes tooth decay is true, but as a result of it depleting nutrients from the body, not because bacteria eat it and produce acid that ruins your teeth.

“Other dental pioneers” appears to be a reference to Dr. May Mellanby and Dr. Edward Mellanby (who discovered vitamin D). These two doctors did a lot of work on the effect of vitamins on tooth structure and decay. The graph, which comes from (http://wholehealthsource.blogspot.co.uk/2009/03/reversing-tooth-decay.html) has been reproduced in a large number of other online articles making claims similar to those made by Natural News. I must have seen it in at least six or seven articles. It is based on the summary of Dr. May Mellanby et al’s series of experiments done on children in hospitals, and, as far as I can tell, seems to be an accurate representation. Except for one crucial ambiguity. The graph uses the word “healing” (unqualified), in the context of “cavities”, neglecting to mention the difference between microcavities (lesions of softened, demineralised enamel) and true cavities – actual holes in the enamel. While softened and weak enamel can remineralise, it cannot grow back, as explained earlier in this note. I will say it again: this crucial difference between the early and late stages of tooth decay is something that is systematically ignored by all the web pages advising readers to ditch the dentist in favour of “natural” cures for “cavities”, a term which they fail to qualify. Some points on the Mellanby studies:

Supplementation of vitamin D (which is needed for absorption of calcium, a major component of teeth, as discussed above) was indeed found to have an ameliorative effect on dental caries, and the recommendation is made, in the concluding summary, that sufficient vitamin D and calcium should be consumed by mothers during pregnancy and by offpring from birth.

But the amelioration should not be, and was not, described by Mellanby simply as the “healing” of cavities, as it is in all these over-zelous articles. The improvements seen in Mellanby’s experiments were:

hardening of carious lesions on the enamel (ie. remineralisation of microcavities, something accounted for uncontroversially within mainstream dentistry) – the word “healing”, out of context, is misleading, especially when the picture presented at the top of the NN the article (and others) is one of multiple, plainly visible, gaping holes in the enamel surfaces of a set of teeth.

The laying down of tertiary protective dentin (dentin being the calcified tissue just below the enamel) in cavities that had already penetrated the enamel. Again, the observation that this response can occur in teeth, arresting the development of caries, is encompassed by modern dental theory. However, there is still debate surrounding how commonly and under what circumstances this occurs. This ‘laying down’ of new dentin, when it occurs, is achieved by the living pulp (remember, dentin is dead tissue). However, this new dentin does not extend very far, and is irregular in structure and far less dense than primary or secondary dentin*, so extremely vulnerable to further decay.

Whereas, across all the other diets studied experimentally by Mellanby, carbohydrate content was kept constant, carbohydrate content was considerably lowered in the cereal-free (low phytic acid) diet. Now that we know about the role of fermentable carbohydrates in tooth decay, this should be flagged up as confounding factor in the experiment’s results and the author’s conclusion regarding the detrimental effect of phytic acid on teeth, an idea which is so popular in current-day articles on natural “healing” of tooth cavities, as well as in “paleo” circles. Phyates are now not considered to have a detrimental effect on teeth. (In fact, when isolated from foods, they have even been found to have an anti-caries effect, though this doesn’t carry through to when they are eaten as an intrinsic component of food.)

Mellanby herself was clear in pointing out that, even on a high-vitamin D diet, “caries is not arrested in all children”, saying that it “appeared that there might well be dietic factors apart from vitamin D influencing the carious process”, and recognising “that some local chemico-parasitic condition in the mouth might explain the continued activity of caries at some points”. She was right, of course – “chemico-parasitic” being a rather apt way to describe the condition imposed by the presence of lactic acid-producing bacteria.

Again, this work was done during a time before vitamin-fortification of cereals and processed carbohydrates, before sugar was identified as the main causal factor in tooth decay, before water fluoridation, and during a time when, accordingly, tooth decay was rife.

The full text version of the report on all four experiments conducted by Mellanby et al. on tooth decay progression in children, from which the graph is taken, can be found here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2520490/?page=3. In fact, all of the Mellanby articles are available online in full.

The food remedies that can heal cavities and tooth decay

In order to restore the ratio of calcium and phosphorus in our blood, and to enable minerals to bond to our teeth, it is not enough to just avoid eating too many sweet or processed foods. We must also eat health-building foods, containing copious amounts of minerals and vitamins that will build a glassy hard tooth structure.

Gelatin – if you don’t have time to make bone broth, this is a good alternative and is great for gums and digestion.

Now go get your pearly white smile back.

The idea that every one of us needs to be working to “restore” the ratio of calcium and phosphorus in our blood has no basis. Aside from being the conclusion of an article deliberately based on anachronistic theory from the 1920s and 30s (and loosely, at that), in general, people who eat reasonable diets based on standard dietary recommendations have no reason to believe that they are suffering from nutritional deficiencies or inbalances. Claims that modern dentistry dismisses the importance of nutrition for healthy teeth are false. Evidence points to the importance of nutrition in the pre-eruptive stage, when teeth are forming, and deficiencies in (for example) vitamin D and A, as well as protein energy malnutrition, have all been linked with poor enamel composition (enamel hypoplasia), which increases susceptibility to tooth decay (see following reference). Furthermore, other nutrient deficiencies are recognised to interfere with saliva composition and quantity (http://ajcn.nutrition.org/content/78/4/881S.full), minimising its protective effect. But in healthy people who eat a normal, balanced diet, in the post-eruptive stage, by far the most important cause of tooth decay is sugar consumption. The authors of the articles addressed in this note offer dental advice but, in so doing, clearly demonstrate that they are neither qualified nor equipped to do so. When seeking out advice on how to maximise the health of your teeth, be sure to check for accreditation by dentists. If you think you’re at risk of being subjected to unnecessary drilling and filling, ask your dentist whether remineralisation with fluoride therapy is a possible alternative. If you still suspect him/her of ‘over-enthusiasm’, go and get a second opinion. But don’t abandon dental appointments in favour of diet regimes invented in the 1930s, before the era of food fortification, water fluoridation, or an understanding of sugar’s role in tooth decay.

*These experiments were conducted in the 20s and 30s. At that time, what is now called tertiary dentin was then known as secondary dentin. The new category reflects the greater understanding dentists now have of tooth structure and function. Thanks to dentist Adrian Stewart, who provided the following explanation in a comment: Secondary dentin is laid down on the inner wall of the dentin throughout the life of the pulp. Dentin is tubular in structure (diameter of approx. 1 micron) with an ondontoblast (the cell that makes dentin and secondary dentin) at the interface of the pulp and he dentin tubule, with a cell process extending into the tubule. Decay entering the dentin leads to death of this ondontoblast, which is replaced by a prto-ondontoblast from pluripotent stem cells within the dental pulp. These then lay down irregular tertiary dentin, which is nowhere near as dense as primary or secondary dentin but acts as a basic defense against the decay process.